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Reversal of hypertrophy: an active biologic process
D Susic1, E Nuñez, E D Frohlich
1Division of Hypertension Research, Alton Ochsner Medical Foundation, New Orleans, LA 70121, USA.
Current Opinion in Cardiology
|September 1, 1995
Summary
Left ventricular hypertrophy involves more than just blood pressure. Reversing it in animals shows benefits, but human studies need more evidence to confirm reduced cardiovascular risk.
Area of Science:
- Cardiology
- Molecular Biology
- Physiology
Background:
- Left ventricular hypertrophy (LVH) development and reversal are complex.
- Hemodynamic load is not the sole determinant of LVH.
- Multiple humoral factors influence cardiac myocyte and non-myocyte growth.
Purpose of the Study:
- To explore factors beyond hemodynamic load in LVH.
- To investigate the potential benefits of LVH reversal.
- To assess the clinical significance of reducing cardiac mass.
Main Methods:
- Review of in vivo, in vitro, and genetic studies.
- Identification of humoral agents affecting cardiac cell mitogenesis.
- Analysis of animal models and human studies on LVH reversal.
Main Results:
- Identified humoral factors include renin-angiotensin system, norepinephrine, endothelins, TGF-β, IGF, bradykinin, prostaglandins, and nitric oxide.
- Animal studies suggest LVH reversal may decrease mortality and improve cardiac function.
- Human studies provide less conclusive evidence on the benefits of reducing LV mass.
Conclusions:
- LVH is influenced by a complex interplay of factors beyond hemodynamics.
- Reversal of LVH in animal models shows promising outcomes.
- Further human research is required to establish the clinical benefits of LV mass reduction in mitigating cardiovascular risks.